Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
192 Cards in this Set
- Front
- Back
|
what are the 3 structures found in the carotid sheath?
|
1. internal jugular vein (lateral)
2. common carotid artery (medial) 3. vagus nerve (posterior) |
|
|
what artery supplies the SA and AV node in most cases?
|
RCA
|
|
|
what aretery supplies the inferior portion of the left ventricle?
|
RCA
|
|
|
which artery is most likely to become occluded and what does it supply?
|
LAD which supplies the anterior interventricular septum
|
|
|
enlargement of which part of the heart can cause dysphagia or hoarsness and why?
|
enlargement of the left atrium because it lies most posterior, just anterior to the esophagus and trachea
|
|
|
what 3 pathologic processes could be heard at the right second intercostal space? (aortic area)
|
1. aortic stenosis
2. flow murmur 3. aortic valve clerosis |
|
|
what 2 pathologic processes could be heard at the left second intercostal space? (pulmonic area)
|
1. pulmonic stenosis
2. flow murmur |
|
|
what 4 pathologic processes could be heard at the 4th intercostal space? (tricuspid area)
|
1. tricuspid regurgitation
2. ventricular septal defect (diastolic murmur) 3. tricuspid stenosis 4. atrial septal defect |
|
|
what 2 pathologic processes could be heard at the 5 intercostal space along the midclavicular line? (mitral area)
|
1. mitral regurgitation (diastolic murmur)
2. mitral stenosis |
|
|
what would a pulmonary flow murmur (increased flow through pulmonic valve during systole) and a diastolic rumble indicate?
|
ASD
|
|
|
what is the equation for cardiac output?
|
stroke volume x HR
|
|
|
how is CO calculated using ficks principle?
|
(rate of O2 consumed)/(PO2a-PO2v)
|
|
|
what are the 2 way in which MAP can be measured?
|
1. CO x TPR
2. 2/3 diastolic + 1/3 systolic pressure |
|
|
how is pulse pressure calculated?
|
systolic pressure - diastolic pressure
|
|
|
what are the 2 ways that stroke volume can be measured?
|
1. CO/HR
2. EDV - ESV |
|
|
what 4 mechanisms will increase heart contractility?
|
1. catecholamines (increase activity of Ca+ pump)
2. increase intracellular Ca+ 3. decrease extracellular Na+ 4. increase intraceullular Na+ (digitalis) |
|
|
what 5 mechanisms can decrease heart contractility?
|
1. Beta-1 blockade
2. HF 3. acidosis (severely decreases calcium release below 6.5) 4. hypoxia 5. non-dihydropyridine Ca2+ channel blockers |
|
|
give an example of a venodilator?
|
one would be nitroglycerine
|
|
|
give and example of a vasodilator?
|
one would be hydralazine
|
|
|
how is the ejection fraction calculated?
|
SV/EDV: remember that SV = EDV-ESV
|
|
|
what is the cutoff for a normal ejection fraction?
|
greater than or equal to 55%
|
|
|
what causes the S1 sound and where will it be heard best?
|
closing of the mitral and tricuspid valves heard best at the mitral area
|
|
|
what causes the S2 sound and where will it be heard best?
|
closing of the aortic and pulmonic valves heard best over the left sternal border
|
|
|
what causes the S3 sound?
|
caused by rapid filling of ventricles due to increase filling pressure
|
|
|
what causes the S4 sound?
|
caused by high atrial pressure assoicated with ventricular hypertrophy
|
|
|
the venous A wave corresponds to what heart action?
|
R atrial contraction
|
|
|
the venous C wave corresponds to what heart action?
|
R ventricular contraction
|
|
|
the venous V wave corresponds to what heart action?
|
filling of right atria increasing pressure as tricuspid vavle is closed
|
|
|
which valve is closing first in S2 splitting?
|
the aortic valve - exacerbated by inspiration
|
|
|
what causes widened splitting of S2?
|
pulmonic stenosis
|
|
|
what causes fixed splitting of S2? (widened splitting without difference between inspiration and expiration)
|
ASD
|
|
|
if S2 split has pulmonic valve closing before the aortic valve what is the problem?
|
aortic stenosis
|
|
|
holosystolic, high-pitched "blowing murmur" describes?
|
mitral/tricuspid valve regurgitation
|
|
|
crescendo-decrescendo systolic ejection murmur following an ejection click indicated?
|
aortic stenosis
|
|
|
holosystolic, harsh-sounding murmur that is loudest at tricuspid area describes?
|
VSD
|
|
|
late systolic murmur with midsystolic click indicates?
|
mitral prolapse
|
|
|
what is the most frequent valvular lesion?
|
mitral prolapse
|
|
|
immidiate high-pitched "blowing" diastolic murmur with a widened pulse pressure when its chronic indicates?
|
aortic regurgitation
|
|
|
delayed rumbling late diastolic murmur following an open snap + LA > LV pressure
|
mitral stenosis
|
|
|
how can tricuspid stenosis be differentiated from mitral valve stenosis?
|
tricuspid valve stenosis will be louder upon inspiration
|
|
|
a constant maching-like murmur is consistent with?
|
PDA
|
|
|
why is cardiac tissue sometimes referred to as a syncitium?
|
the muscle cells are connected by gap junctions so that depolarizing waves can spread between cells
|
|
|
what does the P-wave represent?
|
atrial depolarization
|
|
|
what does the PR interval describe?
|
conduction delay through av node normally less than 200 milliseconds
|
|
|
what does the QRS complex describe?
|
ventricular depolarization normally less than 120 msec
|
|
|
what does the QT interval describe?
|
mechanical contraction of the ventricles
|
|
|
what does the T wave describe?
|
ventricular repolarization
|
|
|
at what point in the electrocardiogram does atrial repolarization occur?
|
during the QRS complex
|
|
|
what does the ST segment describe?
|
it should lie on the isoelectric line and represents the depolarized state of the ventricles
|
|
|
what is a U wave?
|
small dip after the T-wave representing hypokalemia resulting in bradycardia
|
|
|
what is the name of the ECG finding that shows ventricular tachycardia characterized by shifting sinusoidal waveforms?
|
torsades de pointes
|
|
|
what can predispose a patient to torsades de pointes?
|
anything that prolongs the QT interval
|
|
|
what is so dangerous about torsades de points ECG finding?
|
if not corrected it can lead to V-fib
|
|
|
what is the etiology of delta waves and where do they show up on ECG?
|
caused by Wolff-Parkinson-White syndrome and show up as a early depolarization of the ventricles evidenced by premature initiation of the QRS complex
|
|
|
what condition does Wolff-Parkinson-White syndrome sometimes cause by altering the conduction timing through the AV node?
|
allows for formation of reentry depolarizations leading to supraventricular tachycardia
|
|
|
prolonged PR interval (>200 msec) indicated what problem?
|
1st degree AV block
|
|
|
progressive lengthening of the PR interval until a beat is dropped (P wave without resultant QRS) indicates?
|
Mobitz type 1
|
|
|
dropped beats that are not preceded by PR interval changes is called?
|
Mobitz type 2
|
|
|
when atria and ventricles are beating regularly but independent of each other, this is termed?
|
3rd degree heart block = complete block at the AV node
|
|
|
how does activation of the renin-angiotensin system by JGA increase MAP?
|
1. forms angiotensin II - potent vasoconstriction
2. causes release of aldosterone which increases blood volume |
|
|
what causes aortic arch baroreceptors to transmit signals to the medulla?
|
High pressure only
|
|
|
what causes carotid sinus baroreceptors to transmit signals to the medulla?
|
BOTH high and low pressure
|
|
|
what is the cushing's triad? what causes it to happen?
|
1. hypertension
2. bradycardia 3. respiratory depression |
|
|
where does the largest share of cardiac output go?
|
liver
|
|
|
which tissue has the highest blood flow per gram of tissue?
|
kidney
|
|
|
how can left atrial pressure be measured?
|
PCWP pulmonary capillary wedge pressure - normally around <12
|
|
|
what occurs during hypoxia in the lung vasculature?
|
vasocontriction - exact opposite of the rest of the body
|
|
|
how is the net filtration (Pnet) calculated? (starling forces)
|
Pnet = [(Pc-Pi)-((pi)c - (pi)i)]
|
|
|
what are the 5 T's of tetralogy of fallot?
|
1. tetralogy of fallot
2. transposition of great vessels 3. truncus arteriosus 4. tricuspid atresia 5. TAPVR = total anomalous venous return |
|
|
what is the most common cause of cyanosis?
|
tetralogy of fallot
|
|
|
what is the most common congenital anomaly in the heart?
|
VSD
|
|
|
what drug is given to close a PDA?
|
indomethacin
|
|
|
describe the flow of blood in a longstanding VSD?
|
instead of flowing left to right the opposite happens because pulmonary pressure is higher than L ventricular pressure and pulmonic valve stenosis adds to this
|
|
|
what is the sign that the flow of blood has reversed from left to right into a right to left heart shunt?
|
cyanosis - why left to right heart shunts are called blue kids instead of blue babies
|
|
|
what is the name given shunt reversal that happens with long to VSD, ASD, and PDA?
|
Eisenmenger's syndrome
|
|
|
what are the 4 complications of an untreated tetralogy of fallot?
|
1. pulmonary stenosis (most important determinant of prognosis)
2. RVH 3. Overriding aorta 4. VSD Acronym = PROVe |
|
|
when a heart is referred to as boot shaped what does this mean?
|
right ventricular hypertrophy
|
|
|
what will patients with tetralogy of fallot do to improve cyanotic symptoms?
|
they will squat to increase MAP which will decrease the flow of blood from a R -> L
|
|
|
describe what happens in coarctation of the aorta in infants?
|
aortic stenosis proximal to the ductus arteriosus leads to the right heart supplying the lower body via ductus arteriosus and left heart supply upper body via the proximal part of the aorta
|
|
|
what genetic abnormality is coarctation of the aorta associated with?
|
Turner's syndrome
|
|
|
describe what happens in adult type coarctation of the aorta?
|
aortic stenosis after the ductus arteriosus leading to notching of the ribs (enlarged high pressure collateral arteries causing notching in ribs), HTN of upper extremities, and weak pulses in lower extremities
|
|
|
what keeps the ductus arteriosus open?
|
PGE2 (prostaglandin E2) and low O2 tension
|
|
|
describe the defects found with 22q11 syndromes? (2)
|
1. Truncus arteriosus
2. Tetralogy of Fallot |
|
|
describe the defects found with Down syndrome? (3)
|
1. ASD
2. VSD 3. AV septal defects (endocardial cushion defect) |
|
|
describe the defects found with congenital rubella? (3)
|
1. septal defects
2. PDA 3. pulmonary artery stenosis |
|
|
describe the defects found with Turner's syndrome? (1)
|
coarctation of the aorta
|
|
|
describe the defects found with Marfan's syndrome? (1)
|
late aortic insufficiency
|
|
|
describe the defects found with offspring of a diabetic mother? (1)
|
transposition of great vessels
|
|
|
calcification in the media of arteries, especially radial or ulnar that is usually benign is called? ("pipestem" arteries)
|
Monckeberg
|
|
|
Hyaline thickening of small arteries in essential HTN is called?
|
arteriolosclerosis
|
|
|
patient presents with tearing chest pain radiating to his back. AV nicking is present upon ophthalmologic observation. What is this?
|
Aortic disection
|
|
|
describe the locations from most frequent to least for atherosclerotic plaques?
|
abdominal aorta > coronary artery > popliteal artery > carotid artery
|
|
|
what is the most likely cause of stable angina (occurs with exertion?
|
atherosclerosis
|
|
|
whats is the most likely cause of intermittent angina that occurs while the patient is at rest?
|
prinzmetal's variant angina (coronary artery spasm)
|
|
|
if a patient complains of worsening chest pain while at rest, what is the likely etiology?
|
unstable/crescendo angina caused by a thrombosis which has not cut off enough blood supply to cause necrosis, but is increasingly depriving cardiac tissue of oxygen
|
|
|
what is the most common cause of MI?
|
acute thrombosis of coronary arteries due to atherosclerosis
|
|
|
what is the most common cause of sudden cardiac death (within 1 hour)?
|
lethal arrhythmia - ventricular tachycardia for example
|
|
|
what are the 3 most common sites for coronary artery occlusion causing MI? (list from highest frequency to lowest)
|
LAD>RCA>circumflex
|
|
|
if microscopic observation of of cardiac tissue reveals contraction bands and the beginning of neutrophilic emigration into a MI site, how long has it been since the MI?
|
4-24 hours
|
|
|
describe the appearance of an MI after 1 day?
|
dark mottling; pales with tetrazolium stain (lack of cellular respiration)
|
|
|
when is risk for arrhythmia the greatest after MI?
|
2-4 days
|
|
|
when does the bulk of neutrophil emigration occur after MI?
|
2-4 days
|
|
|
when does hyperemia occur after MI?
|
2-4 days after MI blood vessels dialte flooding the area with blood bringing neutrophils to the site of MI. Causes coagulation necrosis of muscle.
|
|
|
when is the maximal risk for rupture of an MI?
|
10 days after neutrophils have cleared most of the necrotic tissue away and a scare has not yet been formed
|
|
|
when do macrophages appear at site of MI?
|
5-10 days after MI
|
|
|
describe the appearance of an MI at 7 10 days?
|
hyperemic border with yellow-brown softening (indentation)
|
|
|
describe the appearance of an MI at 7 weeks?
|
grey-white contracted scare
|
|
|
what is the gold standard for MI diagnosis within the first 6 hours?
|
ECG
|
|
|
what is the most specific serum protein marker of MI and how long is it detectable?
|
Troponin I - as soon as 4 hours post-MI and lasts for 7-10 days
|
|
|
what are the ECG findings indication a transmural MI?
|
1. ST segment elevation
2. Q-waves |
|
|
ST segment depression on ECG indicates?
|
subendocardial MI (only muscle adjacent to endocardium, the least perfused areas)
|
|
|
what is the immediate life threatening result of ventricular rupture post MI?
|
cardiac tamponade
|
|
|
what are the 3 complications of ventricular aneurysm?
|
1. decreased CO
2. arryhthmia 3. embolus formation |
|
|
when is a friction rub most likely to be heard and what is it caused by (post MI)?
|
3-5 days post MI - caused by fibrinous pericarditis
|
|
|
what is Dressler's syndrome?
|
autoimmune phenomenon resulting in fibrous pericarditis several weeks post-MI
|
|
|
what are the 3 types of cardiomyopathies?
|
1. dilated
2. hypertrophic 3. restrictive/obliterative |
|
|
what is the most common cardiomyopathy?
|
dilated
|
|
|
what are the causes of dilated cardiomyopathy?
|
ABCCCDp
1. Alcohol 2. Beriberi 3. Coxsackie B virus 4. Cocain 5. Chagas' 6. Doxorubicin 7. Peripartum |
|
|
Hypertrophic cardiomyopathy most commonly involves what part of the heart?
|
Interventricular septum
|
|
|
what is the genetics of hypertrophic cardiomyopathy?
|
AD - 50% of cases are hereditary
|
|
|
what would you be concerned about if you found a loud S4, strong apical impulses, and a systolic murmur on a 22 year old marathon runner?
|
hypertrophic cardiomyopathy
|
|
|
what are the two drugs that are recommended for the treatment of hypertrophic cardiomyopathy?
|
1. Beta-blockers
2. non-dihydropyridine calcium channel blockers |
|
|
amyloidosis or sarcoidosis would cause this type of cardiomyopathy?
|
restrictive/obliterative
|
|
|
what is endocardial fibroelastosis and what patient population does it occur most frequently in?
|
thick fibroelastic tissue in endocardium of young children causing obstructive/obliterative cardiomyopathy
|
|
|
what is Loffler's syndrome?
|
endomyocardial fibrosis with a prominent eosinophilic infiltrate causing restrictive/obliterative cardiomyopathy
|
|
|
what is the most likely cardiac complication of hemochromatosis?
|
restrictive/obliterative cardiomyopathy
|
|
|
aside from left heart failure, right heart failure is most commonly caused by?
|
cor pulmonale
|
|
|
what is Virchow's triad and what does it predispose one to?
|
1. stasis
2. hypercoagulability 3. endothelial damag Risk for formation of DVT and possible PE |
|
|
what are the signs and symptoms of bacterial endocarditis?
|
Bacteria FROM JANE
-Fever -Roth spot's -Osler's nodes -Murmur (new onset) -Janeway lesions -Anemia -Nail-bed hemorrhage -Emboli |
|
|
what is the most likely cause of acute bacterial endocarditis?
|
S. aureus - large vegetations on previously normal valves
|
|
|
what is the most likely cause of subacute endocarditis?
|
Strep viridans - small vegetations on diseased or congenitally abnormal valves
|
|
|
which valve is most frequently effected by bacterial endocarditis?
|
mitral
|
|
|
which valve is most likely effected in bacterial endocarditis in an IV drug user?
|
the tricuspid valve
|
|
|
verrucous vegetations on BOTH sides of the valve is indicative of this disorder? what is the underlying disease causing this disorder?
|
Libman-Sacks endocarditis - caused by SLE
SLE causes LSE |
|
|
Aschoff bodies (granuloma with giant cells) and Anitschkow's cells (activated histiocytes) indicate what process?
|
Rheumatic heart disease
|
|
|
what are the signs and symptoms of rheumatic heart disease?
|
FEVERSS
-fever -erythemia -Valvular damage (most likely mitral) -ESR increased -Red-hot joints (polyarthritis) -Subcutaneous nodules (Aschoff bodies) -St Vitus' dance (chorea) |
|
|
what is pulses paradoxus (kussmaul's sign)? what emergency situation is it usually associated with?
|
increased pulses upon expiration, decreased pulses on inspiration - cardiac tamponade
|
|
|
what are causes of serous pericarditis? (4)
|
1. SLE
2. rheumatoid arthritis 3. viral infections 4. uremia |
|
|
what are the 3 causes of fibrinous pericarditis?
|
1. Uremia
2. MI (dressler's syndrome) 3. rheumatic fever |
|
|
what are the 2 causes of hemorrhagic pericarditis?
|
1. TB
2. malignancy esp. melanoma |
|
|
what is the most common primary tumor of the heart in adults? where do the occur the most?
|
myxoma, atria (esp L)
|
|
|
what is the most common primary tumor of the heart in children? what disorder are they most associated with?
|
rhabdomyomas - tuberous sclerosis
|
|
|
what is the most common heart tumor?
|
mets from other tumor sites (melanoma or lymphoma)
|
|
|
increased jugular venous pressure upon inspiration is known as? what two pathologic problems with the heart might result in this finding?
|
Kussmaul's sign
1. cardiac tumors 2. cardiac tamponade |
|
|
Patient presents with recurrent nosebleeds and skin discoloration. Many arteriovenous malformations in small vessels are diffusely present. What is it?
|
Osler-Weber-Rendu syndrome a.k.a. hereditary hemorrhagic telangiectasia
|
|
|
Osler-Weber-Rendu syndrome has what inheritance pattern?
|
AD
|
|
|
what disorder is characterized by a triad of necrotizing vasculitis, necrotizing granulomas in lungs and upper airway, and necrotizing glomerulonephritis?
|
Wegener's granulomatosis
|
|
|
A patient is positive for cANCA antibodies, has large nodular densities in chest X-ray, and has red cell casts present in urine analysis. What do they have?
|
Wegener's granulomatosis
|
|
|
what is the treatment for wegener's granulomatosis?
|
cyclophosphamide + corticosteroids
|
|
|
what disorder presents just like Wegener's granulomatosis but lack granulomas and has p-ANCA antibodies?
|
microscopic polyangiitis
|
|
|
A patient has granulomatous vasculitis with eosinophilia. Patient is positive for p-ANCA. Only small vessels are affected with this vasculitis. What do they have?
|
Churg-Strauss syndrome
|
|
|
What is the congenital vascular disorder affecting capillary sized vessels that presents with port-wine stains on face and leptomeningeal aniomatosis?
|
Sturge-Weber disease
|
|
|
what is the most common childhood systemic vasculitis?
|
Henoch-Scholein purpura
|
|
|
A child presents with skin rash, arthralgia, intestinal hemorrhage evidenced by melena, and a recent URI. What does this child have?
|
Henoch-Scholein purpura
|
|
|
what is the triad of Henoch-Schonlein purpura?
|
1. skin
2. joints 3. GI |
|
|
what vessels are affected in Buerger's disease?
|
small and medium sizes
|
|
|
a thrombosing vasculitis seen in heavy smokers which may lead to gangreen is?
|
Beurger's disease
|
|
|
intermittent claudication + superficial nodular phlebitis + Raynauds phenomenon + severe pain in affected part = ?
|
Beurgers disease
|
|
|
what is the treatment of Beurger's disease?
|
stop smoking
|
|
|
what is the mechanism of action for hydralazine?
|
increases cGMP which results in smooth muscle relaxation (vasodilator of arterioles which reduced afterload)
|
|
|
what is the DOC for hypertension in pregnancy? (2 drugs)
|
Hydralazine + methyldopa
|
|
|
what is the important side effect of hydralazine that makes it unsuitable for angina/CAD patients?
|
can cause reflex tachycardia
|
|
|
what is the mechanism of action for minoxidil?
|
K+ channels opener - hyperpolarizes and relaxes vascular smooth muscle
|
|
|
what toxicity can result from the use of minoxidil?
|
hypertrichosis and pericardial effusion
|
|
|
what are the indications for hydralazine?
|
severe hypertension and CHF
|
|
|
what are the indications for minoxidil?
|
severe HTN
|
|
|
what are the 3 popular Ca+ channel blockers?
|
1. Nifedipine
2. verapamil 3. diltiazem |
|
|
list in order of most potent to least potent the effects of these 3 Ca+ channel blockers on vascular smooth muscle?
1. nifedipine 2. verapamil 3. diltiazem |
nifedipine > diltiazem > verapamil
|
|
|
list in order of most potent to least potent the effects of these 3 Ca+ channel blockers on the heart?
nifedipine verapamil diltiazem |
verapamil > diltiazem > nifedipine
|
|
|
describe the mechanism of action of nitroglycerine / isosorbide dinitrate?
|
cause vasodilation by releasing NO into vascular smooth muscle -> increase cGMP -> causes smooth muscle relaxation (HAS MUCH MORE EFFECT ON VEINS THAN ARTERIES = Decreases PRELOAD)
|
|
|
tachycardia, hypotension, flushing, and headache are the toxic effects of which heart medication?
|
Nitroglycerin
|
|
|
what are the 3 medications used to manage malignant HTN?
|
1. nitroprusside
2. fenoldopam 3. diazoxide |
|
|
what is the mechanism of action for nitroprusside?
|
short acting - causes release of NO into vascular smooth muscle increasing cGMP
|
|
|
what is mechanism of action for fenoldopam?
|
D1 receptor agonist - relaxes renal vascular smooth muscle increases filtration
|
|
|
what is the mechanism of action for diazoxide?
|
K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle
|
|
|
List the effect that nitrates (venodilator), beta-blockers (arteriodilator), and nitrates+beta blockers have on end diastolic volume?
|
Nitrates: decrease
Beta-blockers: increase Both: no effect or decrease |
|
|
List the effect that nitrates (venodilator), beta-blockers (arteriodilator), and nitrates+beta blockers have on blood pressure?
|
Nitrates: decrease
Beta-blockers: decrease Both: decrease |
|
|
List the effect that nitrates (venodilator), beta-blockers (arteriodilator), and nitrates+beta blockers have on contractility?
|
Nitrates: increase
Beta-blockers: decrease Both: decrease |
|
|
List the effect that nitrates (venodilator), beta-blockers (arteriodilator), and nitrates+beta blockers have on HR?
|
Nitrates: increase
Beta-blockers: decrease Both: decrease |
|
|
List the effect that nitrates (venodilator), beta-blockers (arteriodilator), and nitrates+beta blockers have on Ejection time?
|
Nitrates: increase
Beta-blockers: decrease Both: little or no effect |
|
|
List the effect that nitrates (venodilator), beta-blockers (arteriodilator), and nitrates+beta blockers have on Ejection time?
|
Nitrates: decrease
Beta-blockers: decrease Both: greatly decrease |
|
|
the effects of nifedipine are similar to beta-blocker or nitrates?
|
nitrates
|
|
|
the effects of verapamil are similar to beta-blocker or nitrates?
|
beta-blocker
|
|
|
what is the mechanism of action of HMG-CoA reductase inhibitors?
|
inhibit cholesterol precursor, mevalonate
|
|
|
what is the mechanism of action of Niacin in lower lipids?
|
inhibits lypolysis in adipose tissue which reduces hepatic VLDL secretion into circulation
|
|
|
what is the mechanism of action of bile acid resins in lower lipids?
|
bind bile acids keeping them from being reabsorbed causing the liver to use cholesterol to make more
|
|
|
what is the mechanism of action for ezetimibe?
|
block absorption of cholesterol in the small intestine
|
|
|
fibrates such as gemfibrozil, clofibrate, bezafibrate, and fenofibrate have what mechanism of action?
|
upregulate lipoprotein lipase which increases triglyceride clearence
|
|
|
which of the lipid lowering drugs decreases LDL the best?
|
HMG-CoA reductase inhibitors such as lovastatin, pravastatin, simvastatin, and atorvastatin
|
|
|
which lipid lowering drugs increase HDL the most?
|
Niacin - also has good LDL lowering ability and some triglyceride lowering ability making it a very effective drug
|
|
|
which drug lowers triglycerides the most?
|
Fibrates such as gemfibrozil, clofibrate, bezafibrate, and fenofibrate
|
|
|
what is a common side effect of niacin use? what can be done to alleviate it?
|
flushing of the face - give aspirin to reduce
|
